“Rhesus positive” or “Rh-positive” is the term commonly given to individuals whose red blood cells are agglutinated by alloantibodies directed against the D antigen (one of the antigens of the RH system), while “Rhesus negative” or “Rh-negative” refers to individuals whose red blood cells are not agglutinated by said alloantibodies.
Hemolytic disease of the newborn is due, in the majority of cases, to the presence of anti-RhD alloantibodies in an Rh-negative mother (alloimmunization against other antigens of the Rh system is much more rare) which, in an Rh-positive fetus, cause hemolytic anemia requiring either intrauterine blood transfusions or exchange transfusion at birth in severe cases.
Alloimmunization of the mother generally occurs during a previous birth when fetal red blood cells enter the maternal circulation, inducing immunization if the fetus is Rh-positive.
Prevention of hemolytic disease of the newborn consists in giving an Rh-negative mother an injection of anti-RhD antibodies immediately after delivery or miscarriage/abortion.
The anti-rhesus antibodies currently used for this purpose are polyclonal immunoglobulins derived from Rhesus-negative volunteer donors immunized several times against Rh-positive red blood cells.
This poses problems, first regarding the need for a sufficient number of donors to meet demand, and secondly due to the risks of contamination by viruses or other pathogens that may be present in the immunglobulin preparations obtained from the blood of volunteer donors.
While several anti-RhD monoclonal antibodies have been produced to replace the polyclonal antibodies, none is yet available for clinical use (Sibéril et al., Clincial Immunology, 2006, 118:170-179).
The T125 clone produced by rat myeloma YB2/0 cells (known as the T125 YB2/0 clone), described by Sibéril et al., supra (and patent application WO2001/77181) was a promising candidate but might be relatively unstable due to intramolecular rearrangements.